LATE

• Jaundice, renal failure and peripheral neuropathy

DEATH
• Within 24 hours to 4 days
• Headache and delirium CEREBRAL
OEDEMA
• Coma and convulsions
• Secondary to vasodilation and cardiac depression SHOCK
• Tachycardia and hypotension
• 30 mins-2hours after ingestion GIT
• Vomiting, diarrhoea, abdominal pain, burning oesophageal pain
ACUTE POISONING
CLINICAL PRESENTATION
• Sore throat, stomatitis, lacrimation, salivation, OTHER
perspiration, garlic odour, vitiligo and alopecia
• Face and ankle
OEDEMA
• Sensory neuropathy
NEURO
• Hyperpigmentation SKIN
• Hyperkeratosis
• Diarrhoea ABDO
• Abdominal pain
CHRONIC POISONING
CLINICAL PRESENTATION
 TARGET ORGANS

• Vasodilation • Rice water • ATN

with reflex stools • Cortical
arteriolar • Bleeding necrosis
constriction • Protein • Oliguria
• Decreased losing S • Proteinuria
contractility enteropathy EY • Haematuria
T • Gangrene N
AR T D
HE GI KI
 • Palmar erythema • Sensory • Central necrosis
• Local oedema neuropathy • Cirrhosis
• Hyperkeratosis M • Muscle atrophy
• Hyperpigmentation E • Encephalopathy
• Atrophy
• Alopecia
ST
• Brittle nails SY
• Mees’ lines US
O
V R
IN ER VE
SK N LI
 INVESTIGATIONS
Nerve
FBC Electrolytes Urine conduction
studies

Ca
24 hour
Microcytic,
urine Peripheral
hypochromic
collection > neuropathy
anaemia
50mcg
Mg
 SPECIMENS
• Blood
• Urine
• Liver
• Kidney
• Stomach and contents
• Hair
• Nails
 MANAGEMENT
• A, B, C
• Fluid replacement to replace GIT losses
• In acute setting
– Gastric lavage if patient presents rapidly or
radiography shows arsenic still in the stomach
– Whole bowel irrigation with polyethylene glycol
– Chelation therapy
• Dimercaprol
– Haemodialysis
 MANAGEMENT
• Chronic arsenic poisoning
– Causes irreversible damage
– Chelation
• Relives clinical manifestations
• Reduces arsenic stores